The emerging role of nutritional vitamin D in secondary hyperparathyroidism in ckd

Chien Lin Lu, Dong Feng Yeih, Yi Chou Hou, Guey Mei Jow, Zong Yu Li, Wen Chih Liu, Cai Mei Zheng, Yuh Feng Lin, Jia Fwu Shyu, Remy Chen, Chung Yu Huang, Kuo Cheng Lu

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)


In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.

Original languageEnglish
Article number1890
Issue number12
Publication statusPublished - Dec 1 2018


  • Calcimimetics
  • Calcitriol
  • Nutritional vitamin D
  • Secondary hyperparathyroidism

ASJC Scopus subject areas

  • Food Science
  • Nutrition and Dietetics


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